It is universally acknowledged that long non-coding RNAs (lncRNAs) involved in tumorigenesis in human cancers. However, the function and mechanism of many lncRNAs in colorectal cancer (CRC) remain unclear. By analyzing the two sets of CRC-related gene microarrays data, downloaded from the Gene Expression Omnibus (GEO) database and the lncRNA expression in a set of RNA sequencing data, we found that lncRNA SLCO4A1-AS1 was significantly upregulated in CRC tissues. We then collected CRC tissue samples and verified that SLCO4A1-AS1 is highly expressed in CRC tissues. Furthermore, SLCO4A1-AS1 was also upregulated in the CRC cell line. In situ hybridization results showed that high expression of SLCO4A1-AS1 was associated with poor prognosis in patients with CRC. Next, we found that SLCO4A1-AS1 promoted CRC cell proliferation, migration, and invasion. Results of western blotting assays show that its mechanism may relate to the epidermal growth factor receptor (EGFR)/mitogen-activated protein kinase (MAPK) pathway. Therefore, SLCO4A1-AS1 may be a potential biomarker for CRC prognosis and a new target for colorectal cancer therapy.

Colorectal cancer (CRC) is one of the most common cancers worldwide. Recent studies have shown that long non-coding RNAs (lncRNAs) are involved in tumorigenesis and the development of CRC. By constructing a differential lncRNA expression profile, we screened gene chips and found that DNAJC3-AS1 was highly expressed in CRC tissues and was associated with poor prognosis in patients with CRC. Further, we proved through assays such as wound healing, colony formation, and Cell Counting Kit-8 (CCK8) that interfering with DNAJC3-AS1 could reduce the proliferation, migration, and invasion of CRC cells. Mechanically, we found that DNAJC3-AS1 regulates fatty acid synthase to promote the progression of CRC via the epidermal growth factor receptor/phosphatidylinositol 3-kinase/protein kinase B/nuclear factor κB signaling pathway. Therefore, DNAJC3-AS1 may be a new target for the diagnosis and therapy of CRC.